Significant visual impairment and blindness develop in many patients with recurrent optic neuritis (ON) and multiple sclerosis (MS). It is estimated that more than 100,000 MS patients have permanent loss of visual acuity from ON at least as severe as 20/30-20/50. Recovery of acuity after ON to no better than 20/30 is associated with substantial optic nerve damage and troublesome symptoms of visual loss. No treatment has been definitively demonstrated to reverse unresolved visual loss in ON. Observations in the experimental allergic encephalomyelitis animal model of MS and in the Theiler's model of demyelination suggest that immunoglobulins directed against CNS components promote oligodendroglial proliferation and new myelin synthesis. Preliminary studies in inflammatory-demyelinating disease of the human peripheral and central nervous system suggest that the repeated intravenous administration of purified human immunoglobulin (IVIg) is followed by clinical improvement. A recent pilot study, suggests that IVIg administration is followed by improvement in visual function in chronic, steroid unresponsive ON. In this randomized, placebo-controlled, double-blinded clinical trial, we test the hypothesis that IVIg administration results in clinical improvement of apparently irreversibly lost visual function (acuity) in patients with ON in the context of MS. Sixty patients identified as having a fixed, unresolved loss of visual acuity from ON will be randomized to receive either IVIg or placebo (0.1% human serum albumin in 10% maltose) for five days and then once per month for three months (total of 8 infusions). The primary endpoint will be the assessment of whether there has been improvement in visual acuity using a retroilluminated Snellen ETDRS letter chart. Secondary outcomes will include changes in visual fields and visual evoked responses. If IVIg administration is followed by improvement in visual function in ON, this would represent a major therapeutic breakthrough for patients with ON in the context of MS and would suggest that IVIg administration may possibly have a role in reversing neurological dysfunction in inflammatory-demyelinating diseases. This would provide opportunities for the development of new therapies in patients with demyelinating and dysmyelinating disease perhaps by enhancing the potential for myelin repair in the CNS.